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Protein Synthesis in the Liver - Provet Pet Health Information
Nevertheless, in all such conditions, the cessation of alcohol is essential. In this way, you can prevent the liver from further damage. On the other hand, the use of medication will help liver synthesize its damaged cells.
In short, the liver performs a great variety of tasks, ranging from the synthesis, storage and secretion to detoxification of harmful substances. Different secretions are of great metabolic importance. The liver function in digestion is also very significant.
THE LIVER AND PROTEIN SYNTHESIS
Several articles have reported a two- to threefold increased incidence of gallstones in diabetic patients, whereas others have failed to demonstrate a significant association.17,48-52 Gallbladder emptying abnormalities found in diabetic patients may predispose patients to cholelithiasis.53 Secretion of lithogenic bile by the liver in patients with type 2 diabetes probably predisposes them to forming gallstones, but this is likely a result of concomitant obesity rather than a result of the diabetes itself.54 Increased biliary cholesterol saturation has not been demonstrated in insulin-dependent diabetic patients.
APAP toxicity, networks and organ-specific biomarkers. In APAP-induced toxicity, the normal conversion of APAP to non-toxic derivates by glucuronidation and sulfation is overwhelmed. APAP is first oxidized by cytochrome P450 enzymes to a toxic metabolite, N-acetyl-p-benzoquinone-imine (NAPQI) (). Normally, low levels of this highly-reactive electrophile are quickly detoxified by conjugation with hepatic glutathione (GSH). Following APAP overdose, however, the hepatic GSH levels are insufficient to conjugate all of the NAPQI. The surplus forms cysteine adducts to various macromolecules, disrupts numerous critical cellular functions, and elevates innate immune responses which collectively results in centrilobular hepatocyte death (-). Depletion of GSH by NAPQI and its ability to detoxify NAPQI is the major cause of APAP hepatotoxicity (). N-acetylcysteine (NAC), a GSH precursor, is a clinical antidote for excess NAPQI used to treat APAP overdose (). S-adenosyl-L-methionine (SAMe) is a key physiological precursor of GSH production, as well as the methyl donor in most transmethylation reactions. Endogenous hepatic SAMe concentrations drop dramatically after APAP hepatotoxicity (). Administration of SAMe provides comparable protective and therapeutic effects to NAC (,). Interestingly, we observed that three SAMe metabolic enzymes―MAT1A, GNMT, and BHMT decreased in the liver during injury while appearing elevated in the blood. MAT1A catalyzes the synthesis of SAMe(). GNMT and BHMT are two methyltransferases regulating metabolism of S-adenosylhomocysteine (SAH) and homocysteine which are precursors of GSH (-). Loss of these enzymes would cause a significant decrease of SAMe and GSH and could consequently aggravate the liver injury. There was inverse correlation between the protein concentrations in the liver and in the blood for these three proteins, suggesting that the blood proteins were released from stressed hepatocytes or leaked from dead hepatocytes. Therefore, liver-specific blood proteins MAT1A, GNMT, and BHMT might be useful indicators of hepatic SAMe and GSH states and thus have prognostic value for GSH depletion-related hepatotoxicity.
The dominant role of the liver in plasma protein synthesis: ..
Organ-specific blood biomarkers. We propose here a new strategy for identifying biomarkers that will potentially permit early detection, disease stratification, and follow progression―all from blood analyses. The basic concept is that all organs/tissues uniquely synthesize some transcripts and proteins, and that those entering the bloodstream reflect effects on their cognate biological networks during disease progression. These proteins may be secreted, leaked by cell damage/death, or released from cell membranes by proteolysis. This approach has several key features. 1) Selected markers report the affected organ(s). 2) Panels survey a spectrum of networks to report the type of perturbation. 3) When one can identify the cognate biological networks of organ-specific proteins, one can begin to investigate the nature of the disease mechanism. This approach could be very useful in assessing the effects of new drugs on particular organs.
Human APAP-toxicity plasma samples. Ideal hepatic safety markers should be detectable in both preclinical and clinical tests. Eleven leakage markers in our blood signature are liver-specific at both RNA and protein levels in both mouse and human. We checked these markers in human blood samples with APAP toxicity by immunoblotting. Five proteins (BHMT, DPYS, FAH, FBP1, HPD) were detected in liver injury plasma samples, but not in matched normal samples. The other six proteins (ALDH1L1, AGXT, COMT, CPS1, GNMT and MAT1A) could not be detected in any human samples by Western blot (data not shown). We used purified recombinant human proteins as standards and the Li-COR software for estimating concentration. BHMT, DPYS, FAH, FBP1 were found to be in the microgram-per-milliliter range (5.1-64.9 µg/mL), notably higher than ALT (0.22-0.55 µg/mL). HPD was found at a level similar to ALT (Table ). While protein quantitation by immunoblotting is somewhat approximate, it seems likely that these proteins are significantly more abundant in the toxicity samples than ALT. For comparison, we calibrated our enzymatic assays using purified human ALT1 (0.46 IU/µg) and ALT2 (0.08 IU/µg) proteins (OriGene, Rockville, MD). (See : Figure S6.) These assays measured ALT levels in the low microgram-per-milliliter range (0.4-1.2 µg/ml), consistent with the immunoblotting estimates.
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Protein Synthesis by the liver | My Blog
The dynamic profile of sixteen liver-specific protein concentrations reflects the onset and reversal of the histopathology. The four proteins that declined in blood during liver injury ――PLG, retinol binding protein 4, plasma (RBP4), TF and ceruloplasmin (CP) ―― are secretory proteins. These exhibited different temporal concentration profiles (Figure A,B). RBP4 responded first and recovered last, while ceruloplasmin had only marginal response at the time of peak liver damage. Plasminogen and transferrin had intermediate responses. The other 11 proteins exhibited elevated levels during liver injury. Nine were from the cytosol: alanine-glyoxylate aminotransferase (AGXT), aldehyde dehydrogenase 1 family member L1 (ALDH1L1), betaine-homocysteine methyltransferase (BHMT), dihydropyrimidinase (DPYS), fumarylacetoacetate hydrolase (FAH), fructose bisphosphatase 1 (FBP1), Glycine N-methyltransferase (GNMT), 4-hydroxyphenylpyruvic acid dioxygenase (HPD), and methionine adenosyltransferase I alpha (MAT1A). Their temporal profiles were similar to ALT, reflecting a pathological response peaking between 12 and 24 hours then gradually returning to normal in surviving mice (Figure A, C). This reflects directly the destruction of liver cells and their recovery. Distinct temporal profiles were observed for the mitochondrial protein, CPS1, and for membrane-bound catechol-O-methyltransferase (MB-COMT). These elevated earlier than other leakage markers and ALT/AST. The protein profiles at the cellular level differed greatly from the plasma level. Levels of these 11 proteins in the liver lysates declined slightly over the time course, with the exception of MB-COMT, MB-COMT was highly elevated between 24 and 48 hours (Figure D), consistent with liver cell loss or damage.
The Liver and protein synthesis Flashcards | Quizlet
COMT is an APAP response marker. In the early stages, even before ALT/AST and histopathology indicate injury, RBP4 and COMT levels changed significantly (Figure A). Immunoblotting showed the MB-COMT level elevated in both liver tissue and plasma during liver injury (24 hours) (Figure B). The S-COMT protein in mouse liver decreased (in the same manner as the other liver enzymes), whereas MB-COMT increased significantly, especially 24 - 48 hours post-injection (Figure C). In blood, S-COMT could not be detected by immunoblotting under any conditions, but MB-COMT increased significantly in liver injury mouse instances (Figure A). We also checked MB-COMT expression in mouse liver by immunohistochemistry with a specific anti-MB-COMT antibody and found that MB-COMT level increased significantly at 48 hours post-injection. (Figure D)
The dominant role of the liver in plasma protein synthesis
APAP-induced mouse liver injury signature. Temporal profiles of proteins in plasma observed to correlate with level of liver injury. Albumin concentration was not visibly changed. Transferrin, ceruloplasmin, plasminogen and RBP4 levels were seen to decrease with injury. The traditional liver function markers, ALT and AST, exhibited levels elevating with liver injury, as did a number of potentially novel biomarkers. Unless specified otherwise, all relative levels were determined by quantitative immunoblotting and normalized to the mean over the time course. (A) Qualitative plasma profiles for 17 proteins by Western blot. (B) Quantitative plasma profiles for four secretory proteins. (C) Quantitative plasma profiles of ALT and novel biomarkers. ALT indicates injury at 3 hours, peak at 12 hours, and return to baseline at 96 hours. ALT levels here were assayed by enzymatic activity and reported in IU/mL. MB-COMT and CPS1 have apparently different patterns from ALT. (D) Quantitative liver lysate protein profiles of the novel blood biomarkers. Lysate profiles differed greatly from the plasma profiles. The increase in MB-COMT levels was shifted later in time, while the other protein levels are attenuated between 24 and 48 hours.
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